Papers - Ouchi, Takeshi

Generalized eruptive histiocytoma developing into xanthoma disseminatum with central diabetes insipidus

Kobayashi K, Kurihara Y, Yamagami J, Ito J, Shima H, Shimada H, Ichimura C, Ishiko A, Amagai M, Ouchi T

J Dermatol 46 ( 8 ) e281 - e283 2019.08

Joint Work, Accepted,  ISSN  0385-2407

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Patient voice on management of facial dermatological adverse events with targeted therapies: a qualitative study

Yagasaki K, Takahashi H, Ouchi T, Yamagami J, Hamamoto Y, Amagai M, Komatsu H

J Patient Rep Outcomes 3 ( 1 ) 27 2019.05

Joint Work, Accepted,  ISSN  2509-8020

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Gamma-delta T cell large granular lymphocyte leukaemia with multiple cutaneous nodules that showed spontaneous regression

Suzuki C, Hirai I, Nomura H, Ouchi T, Okayama M, Okamoto S, Amagai M, Tanese K, Takahashi H

(J Eur Acad Dermatol Venereol)  33 ( 3 ) e134 - e137 2019.03

Joint Work, Accepted,  ISSN  0926-9959

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Combination of low-dose total skin electron beam therapy and subsequent localized skin electron beam therapy as a therapeutic option for advanced-stage mycosis fungoides

Kinoshita-Ise M, Ouchi T, Izumi E, Kawaguchi O, Nagao K, Amagai M, Funakoshi T

Clin Exp Dermatol 43 ( 4 ) 437 - 440 2018.06

Joint Work, Accepted,  ISSN  0307-6938

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Case of lamotrigine-induced drug adverse reaction under tocilizumab treatment with clinical and virological features of drug-induced hypersensitivity syndrome

Iriki H, Ouchi T, Ito H, Sawada M, Mukai M, Nomura H, Baba Y, Adachi T, Funakoshi T, Amagai M, Takahashi H

(J Dermatol)  45 ( 6 ) 738 - 741 2018.06

Joint Work, Accepted,  ISSN  0385-2407

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Langerhans cells prevent autoimmunity via expansion of keratinocyte antigen-specific regulatory T cells

Kitashima, D. Y. Kobayashi, T. Woodring, T. Idouchi, K. Doebel, T. Voisin, B. Adachi, T. Ouchi, T. Takahashi, H. Nishifuji, K. Kaplan, D. H. Clausen, B. E. Amagai, M. Nagao, K.

EBioMedicine 27   293 - 303 2018.01

Accepted,  ISSN  2352-3964

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Non-pigmenting fixed drug eruption with mixed features of acute generalized exanthematous pustulosis induced by pseudoephedrine: a case report

Fukuda, R. Ouchi, T. Hirai, I. Funakoshi, T. Honda, A. Tanese, K. Tanikawa, A. Amagai, M. Takahashi, H.

Contact Dermatitis 77 ( 2 ) 123 - 126 2017.08

Joint Work, Accepted,  ISSN  0105-1873

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Case of isolated epidermolytic acanthoma: Genetic and immunohistochemical analysis

Adachi, T. Tanese, K. Ouchi, T. Igawa, S. Nakano, H. Ishiko, A.

J Dermatol 43 ( 8 ) 974 - 975 2016.08

Joint Work, Accepted,  ISSN  0385-2407

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Acquired dermal melanocytosis of the face and extremities

Ouchi, T. Ishii, K. Nishikawa, T. Ishiko, A.

Clin Exp Dermatol 41 ( 6 ) 643 - 647 2016.08

Joint Work, Accepted,  ISSN  0307-6938

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EpCAM Expressed by Murine Epidermal Langerhans Cells Modulates Immunization to an Epicutaneously Applied Protein Antigen

Ouchi, T. Nakato, G. Udey, M. C.

J Invest Dermatol 136 ( 8 ) 1627 - 1635 2016.08

Accepted,  ISSN  0022-202X

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Langerhans cells (LCs) induce type 2 antibodies reactive with protein antigens that are applied to murine skin in the absence of adjuvant after extending their dendrites through tight junctions to acquire antigens and migrating to regional lymph nodes. In response to contact sensitizers, epithelial cell adhesion molecule (EpCAM) on LCs promotes LC dendrite mobility and LC migration. In epithelial cells, EpCAM regulates expression and distribution of selected tight junctions-associated claudins. To determine if EpCAM regulates claudins in LC and immune responses to externally applied proteins, we studied conditional knockout mice with EpCAM-deficient LCs. Although LC claudin-1 levels were dramatically reduced in the absence of EpCAM, conditional knockout mice with EpCAM-deficient LCs and control LC dendrites docked with epidermal tight junctions with equal efficiencies and ingested surface proteins. Topical immunization of conditional knockout mice with EpCAM-deficient LCs with ovalbumin led to increased induction of type 2 Ova-specific antibodies and enhanced proliferation of ovalbumin-reactive T cells associated with increased accumulation of LCs in lymph nodes. These results suggest that, in the absence of strong adjuvants, EpCAM-deficient LCs exhibit increased migration to regional lymph nodes. EpCAM appears to differentially regulate LC mobility/migration in the setting of limited inflammation as compared with the intense inflammation triggered by contact sensitizers.

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Hapten-induced lymphadenosis benigna cutis secondary to squaric acid dibutylester sensitization for alopecia areata

Adachi, T. Ouchi, T. Ebihara, T. Ohyama, M.

J Dermatol 41 ( 2 ) 182 - 183 2014.02

Joint Work, Accepted

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ドセタキセルが奏効した進行期乳房外パジェット病の3例

舩越建 福田桂太郎 大内健嗣 横山知明 髙江雄二郎 天谷雅行

臨床皮膚科 67 ( 9 ) 657 - 662 2013.08

Joint Work, Accepted

骨低形成,脂肪萎縮を伴った顔面に生じたBecker母斑症候群の1例

栗原佑一 橋本玲奈 大内健嗣 大山学 海老原全 天谷雅行 石河晃

臨床皮膚科 67 ( 8 ) 607 - 610 2013.07

Joint Work, Accepted

Rheumatoid neutrophilic dermatosisの1例 関節リウマチの病勢との関連について

足立剛也 崎山とも 大内健嗣 髙江雄二郎 安岡秀剛 谷川瑛子

臨床皮膚科 67 ( 7 ) 501 - 505 2013.06

Joint Work, Accepted

Langerhans cell antigen capture through tight junctions confers preemptive immunity in experimental staphylococcal scalded skin syndrome

Ouchi Takeshi, Kubo Akiharu, Yokouchi Mariko, Adachi Takeya, Kobayashi Tetsuro, Kitashima Daniela Y., Fujii Hideki, Clausen Björn E., Koyasu Shigeo, Amagai Masayuki, Nagao Keisuke

Journal of Experimental Medicine 208 ( 13 ) 2607 - 2613 2011.12

ISSN  0022-1007

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<p>Epidermal Langerhans cells (LCs) extend dendrites through tight junctions (TJs) to survey the skin surface, but their immunological contribution in vivo remains elusive. We show that LCs were essential for inducing IgG1 responses to patch-immunized ovalbumin in mice that lacked skin dendritic cell subsets. The significance of LC-induced humoral responses was demonstrated in a mouse model of staphylococcal scalded skin syndrome (SSSS), a severe blistering disease in which the desmosomal protein Dsg1 (desmoglein1) is cleaved by Staphylococcus aureus-derived exfoliative toxin (ET). Importantly, ET did not penetrate TJs, and patch immunization did not alter epidermal integrity. Nevertheless, neutralizing anti- ET IgG ₁ was induced after patch immunization and abolished upon LC depletion, indicating that antigen capture through TJs by LCs induced humoral immunity. Strikingly, the ET-patched mice were protected from developing SSSS after intraperitoneal ET challenge, whereas LCdepleted mice were susceptible to SSSS, demonstrating a vital role for LC-induced IgG1 in systemic defense against circulating toxin in vivo. Therefore, LCs elicit humoral immunity to antigens that have not yet violated the epidermal barrier, providing preemptive immunity against potentially pathogenic skin microbes. Targeting this immunological process confers protection with minimal invasiveness and should have a marked impact on future strategies for development of percutaneous vaccines. © 2011 Ouchi et al.</p>

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A Japanese-specific recurrent mutation and a novel splice site mutation in the LAMC2 gene identified in two Japanese families with Herlitz junctional epidermolysis bullosa

Kouno, M., Ko, R., Shimizu, A., Ouchi Takeshi, Sueoka, K., Masunaga, T., Ishiko, A.

Clinical and Experimental Dermatology 36 ( 4 ) 386 - 392 2011.06

ISSN  03076938

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Background. Herlitz junctional epidermolysis bullosa (H-JEB) is an extremely rare genodermatosis characterized by lethality owing to severe blister formation. We report two unrelated Japanese patients with H-JEB. Genetic analyses detected a single nonsense mutation on the LAMC2 gene in these two patients. Aim. To identify the mutation involved and describe the first reported Japanese recurrent mutation in the LAMC2 gene. Methods. Direct sequencing was performed of DNA from either peripheral blood or fetal cells in amniotic fluid. Reverse transcriptase PCR was used to confirm that an aberrant transcript resulted from the splice site mutation. A haplotype analysis was performed to define the origin of the recurrent mutation. Results. Both patients had blisters and erosions on the trunk and limbs at birth, with nail dystrophy. Patient 1 died as a result of sepsis at 30weeks of age, and patient 2 died as a result of disseminated intravascular coagulation at 20weeks of age. Mutation analysis of the LAMC2 gene revealed that patient 1 was compound heterozygous for a nonsense mutation (p.Cys553X) and a novel splice site mutation (c.2868+1delG), and patient 2 was a homozygous for p.Cys553X. Prenatal diagnosis performed during a subsequent pregnancy in family 2 revealed that this second child was heterozygous for p.Cys553X, and was thus not affected. Haplotype analysis suggested that a p.Cys553X allele derived from the same origin had been independently inherited by these two unrelated families. Conclusions. p.Cys553X in the LAMC2 gene may be a Japanese-specific recurrent mutation as a result of a founder effect, and it may therefore be useful for initial screening in the mutation analysis of H-JEB. © The Author(s). CED © 2010 British Association of Dermatologists.

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A case of blastomycosis-like pyoderma caused by mixed infection of staphylococcus epidermidis and trichophyton rubrum

Ouchi Takeshi, Tamura Mai, Nishimoto Shuhei, Sato Tomotaka, Ishiko Akira

American Journal of Dermatopathology 33 ( 4 ) 397 - 399 2011.06

ISSN  0193-1091

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<p>Blastomycosis-like pyoderma (BLP) is a type of chronic pyoderma characterized histologically by specific epidermal changes namely: pseudoepitheliomatous hyperplasia and intraepithelial abscesses. These epidermal changes are also seen in blastomycosis (referred to as deep dermatophytosis in North America). Here, we describe the case of a 53-year-old male with prurigo nodularis, diabetes, and chronic lymphocytic leukemia who presented with multiple yellowish-red colored papules that coalesced to form a vegetating plaque. In addition to the typical features of BLP, spores with budding were seen histopathologically in a biopsy specimen. Cultures of a skin specimen grew Staphylococcus epidermidis and Trichophyton rubrum. Antibiotic therapy was effective but failed to eliminate the lesion until antifungal therapy using terbinafine was administered concurrently. Past reports suggest that BLP is mainly caused by bacterial infection, but our case suggests that fungal infection can also be involved as the causative organism in BLP. Copyright © 2011 by Lippincott Williams &amp; Wilkins.</p>

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Plectin expression patterns determine two distinct subtypes of epidermolysis bullosa simplex

Natsuga, K., Nishie, W., Akiyama, M., Nakamura, H., Shinkuma, S., McMillan, J.R., Nagasaki, A., Has, C., Ouchi Takeshi, Ishiko, A., Hirako, Y., Owaribe, K., Sawamura, D., Bruckner-Tuderman, L., Shimizu, H.

Human Mutation 31 ( 3 ) 308 - 316 2010.03

ISSN  10597794

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Plectin is a cytoskeletal linker protein that has a dumbbell-like structure with a long central rod and N- and C-terminal globular domains. Mutations in the gene encoding plectin (PLEC1) cause two distinct autosomal recessive subtypes of epidermolysis bullosa (EB): EB simplex with muscular dystrophy (EBS-MD), and EB simplex with pyloric atresia (EBS-PA). Here, we demonstrate that normal human fibroblasts express two different plectin isoforms including full-length and rodless forms of plectin. We performed detailed analysis of plectin expression patterns in six EBS-MD and three EBS-PA patients. In EBS-PA, expression of all plectin domains was found to be markedly attenuated or completely lost; in EBS-MD, the expression of the N- and C-terminal domains of plectin remained detectable, although the expression of rod domains was absent or markedly reduced. Our data suggest that loss of the full-length plectin isoform with residual expression of the rodless plectin isoform leads to EBS-MD, and that complete loss or marked attenuation of full-length and rodless plectin expression underlies the more severe EBS-PA phenotype. These results also clearly account for the majority of EBS-MD PLEC1 mutation restriction within the large exon 31 that encodes the plectin rod domain, whereas EBS-PA PLEC1 mutations are generally outside exon 31. © 2010 Wiley-Liss, Inc.

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Polypoid basal cell carcinoma on the scrotum

Ouchi Takeshi, Sugiura Makoto

Journal of Dermatology 35 ( 12 ) 804 - 805 2008.12

ISSN  0385-2407

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Indeterminate cell histiocytosis successfully treated with ultraviolet B phototherapy

Ishibashi, M., Ouchi Takeshi, Tanikawa, A, Ishiko, A.

Clinical and Experimental Dermatology 33 ( 3 ) 301 - 304 2008.05

ISSN  03076938

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Indeterminate cell histiocytosis (ICH) is a rare disorder, characterized by infiltration of the skin by neoplastic cells that are characteristically positive for S-100 and CD1a, but lack Birbeck's granules. A 75-year-old man presented with a 4-year history of multiple papules on the trunk, limbs, face and neck. Skin biopsy revealed dense infiltration of histiocytic cells that were CD1a+/S100+, but lacked Birbeck's granules. No other abnormality was seen during a general examination including a computed tomography scan of the body, gallium scintigraphy, and an abdominal sonography. Broadband ultraviolet B (UVB) treatment was used for the skin lesions, and partial but almost complete remission was obtained. The case suggests that UVB phototherapy is an option for treatment of ICH. © 2008 The Author(s).

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